Retinal ganglion cell genesis requires lakritz, a zebrafish atonal homolog

Kay, J. N.; Finger-Baier, Karin; Roeser, T.; Staub, W.; Baier, Herwig

doi:10.1016/s0896-6273(01)00312-9

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

Retinal ganglion cell genesis requires lakritz, a zebrafish atonal homolog

MPS-Authors

There are no MPG-Authors in the publication available

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

Kay, J. N., Finger-Baier, K., Roeser, T., Staub, W., & Baier, H. (2001). Retinal ganglion cell genesis requires lakritz, a zebrafish atonal homolog. Neuron, 30(3), 725-736. doi:10.1016/s0896-6273(01)00312-9.

Cite as: https://hdl.handle.net/21.11116/0000-0009-8365-1

Abstract

Mutation of the zebrafish lakritz (lak) locus completely eliminates the earliest-born retinal cells, the ganglion cells (RGCs). Instead, excess amacrine, bipolar, and Muller glial cells are generated in the mutant. The extra amacrines are found at ectopic locations in the ganglion cell layer. Cone photoreceptors appear unaffected by the mutation. Molecular analysis reveals that lak encodes Ath5, the zebrafish eye-specific ortholog of the Drosophila basic helix-loop-helix transcription factor Atonal. A combined birth-dating and cell marker analysis demonstrates that lak/ath5 is essential for RGC determination during the first wave of neurogenesis in the retina. Our results suggest that this wave is skipped in the mutant, leading to an accumulation of progenitors for inner nuclear layer cells.